supra & intra

horizontal conditions

Horizontal Gaze Palsy

• Paresis of conjugate horizontal gaze (may be selective saccadic palsy or affect both saccades and smooth pursuit)

lesion location/ aeitology

• Cortex e.g Frontal Eye Fields– contralateral to lesion (Aetiology commonly stroke)

• Pons– PPRF/ VIN nucleus

1 ½  Syndrome  &

• INO + Horizontal Gaze palsy

• VI N Nucleus (+/ PPRF) + MLF

 Signs: Limited horizontal gaze except for abduction in one eye.

VIII ½ Syndrome

• 1 ½ + VII Nerve palsy

• VI + VII N Nucleus + MLF

• Eight-and-a-Half Syndrome: One-and-a-half syndrome plus facial nerve palsy.

horizontal - INO

Internuclear Ophthalmoplegia

• Limitation of adduction + abducting nystagmus of contralateral eye.  Convergence may be preserved.

• oscillopsia

Lesion site

• Medial Longitudinal Fasciculus (MLF) (commonly Multiple Sclerosis) Convergence may also be affected in more rostral lesions

Variants:

• WEBINO: Bilateral INO.

• INO of Lutz: Reverse INO with abduction deficit.

• Tests: Smooth pursuits and saccades reveal adduction lag; convergence unaffected if MLF is the only affected structure.

likely cause of INO in older pts - stroke

younger pts - MS

Why get nystagmus - repeated signal sent to 6th nerve to get eye to look in adduction but unable to work so get nystagmus instead

Vertical - vgp

Vertical Gaze Palsy

• Paresis of conjugate vertical gaze (Bilateral symmetrical limitations of up/ down gaze)

• In degenerative disease saccades may be affected 1^st followed by smooth pursuit

• Vertical Gaze Centre RiMLF

Degenerative Conditions

• psp - downgaze 1st

  • Progressive Supranuclear Palsy (PSP):

    • Signs: Downward gaze affected, saccadic initiation defect, Bell’s phenomenon absent.

    • Tests: Reduced vertical saccades.

• parkinson’s - upgaze 1st

  • Signs: Hypometric saccades, saccadic intrusions, vertical gaze impairment, postural instability.

  • Lesion: Basal ganglia degeneration.

• corticobasal degeneration

affecting basal ganglia, substania nigria, reticulor formation

Vertical - parinuds

Parinauds Syndrome

• Upgaze palsy

• Convergence retraction nystagmus

 

• Light – near dissociation.

• Pupillary light response impaired with normal near response

• affects the vertical gaze centre and the descending fibres of the pupillary light reflex. Signal for the near response travels more ventrally resulting in light-near dissociation.

• Lesion Location: Dorsal midbrain (e.g., Parinaud’s syndrome).

• Signs: Upgaze palsy, convergence-retraction nystagmus, lid retraction (Collier’s sign), and light-near dissociation.

• Cause: Often due to a pineal gland tumor.

• Tests: VOR improves upgaze; OKN testing induces convergence-retraction.

vertical - tonic gaze

Tonic Downward Gaze (Setting sun sign)

Upgaze paresis, eyes appear driven downwards, lower portion of pupil may be covered by lower eyelid

Distention of cerebral aqueduct affecting vertical gaze centre often seen in babies/ children with increased intracranial pressure/ hydrocephalus

Vertical - double elevator and depressor palsy

Double Elevator Palsy

Monocular elevation deficit (IO & SR u/a)

May have associate ptosis

Need to ^^ from IR restriction (Increase on Dolls head/ Bells reflex retained, -ve FDT)

• Pretectal area of IIIN nucleus often congenital

• Lesion: Affecting the superior rectus and inferior oblique of one eye.

• Signs: Unilateral upgaze defect and hypotropia.

• Tests: Differentiated from Brown's syndrome with forced duction tests and Bell's phenomenon.

Double depressor palsy

Monocular depression deficit (SO & IR u/a)

Rare usually congenital

Reports - bilateral paramedian thalamic infarcts

vertical - skew

Skew deviation

• Vertical deviation may be unilateral or alternating hypertropia -mimic 4th NP

• Deviation reduces by 50% in supine position (upright supine test)

• Torsion features - impaired ocular tilt

• Often associated central vestibular nystagmus

Location

Anywhere within the posterior fossa

Vesibular nuclei (brainstem or occasionally cerebellum)

supranuclear

Signs: Vertical misalignment with torsion + nystagmus downbeat

1. Associated Symptoms:

   • Vertigo or dizziness.

   • Nystagmus (involuntary eye movements).

   • Poor balance or gait instability.

2. Common Causes:

   • Strokes, multiple sclerosis, trauma, or tumors affecting the brainstem or cerebellum.

Smooth pursuit system defect – cog wheel movements /

Inability to track objects smoothly

smooth p pathway

1. Visual Input:

   • Starts in the retina, detecting the moving target.

   • Signal travels via the optic nerve, optic chiasm, and optic tract to the lateral geniculate nucleus (LGN).

   • From the LGN, signals reach the primary visual cortex (V1) in the occipital lobe for processing.

2. Higher Processing (Cortical Areas):

   • Middle Temporal (MT) and Medial Superior Temporal (MST) Visual Areas:

     • Determine the speed and direction of the moving target.

   • Information is sent to the frontal eye fields (FEF) and parietal eye fields, which help initiate and control pursuit movements.

3. Brainstem Integration:

   • Signals are relayed to the pontine nuclei in the brainstem.

   • The cerebellum (flocculus and vermis) refines the movement, ensuring smooth and accurate tracking.

4. Motor Execution:

   • Signals are transmitted to the ocular motor nuclei (CN III, IV, VI) via the medial longitudinal fasciculus (MLF) to coordinate eye movements.

Saccadic palsy/ Oculomotor apraxia

Inability to initiate fast saccadic eye movement, these may be specific to reflexive/ volitional.

Can be congenital

Specific areas of saccadic pathway FEF/ PEF

Degenerative diseases such as dementia may exhibit specific deficits in volitional saccades

1. Initiation:

   • Visual input or voluntary control initiates saccades.

   • Frontal Eye Fields (FEF):

     • Primary area for voluntary saccades.

   • Superior Colliculus:

     • Integrates sensory input and motor commands, especially for reflexive saccades.

2. Signal Transmission to Brainstem:

   • Horizontal Saccades:

     • Controlled by the paramedian pontine reticular formation (PPRF) in the pons.

     • PPRF sends signals to the abducens nucleus (CN VI), activating the lateral rectus of the ipsilateral eye.

     • The MLF transmits signals from CN VI to the contralateral oculomotor nucleus (CN III) to activate the medial rectus of the opposite eye.

   • Vertical Saccades:

     • Controlled by the rostral interstitial nucleus of the MLF (riMLF) in the midbrain.

     • Coordinates signals to the superior and inferior recti and oblique muscles.

3. Cerebellar Refinement:

   • The cerebellum ensures accuracy and amplitude control of saccades.

4. Motor Execution:

   • Final motor signals are sent to the extraocular muscles via CN III, IV, and VI to execute the movement.

Vergence

Convergence

Divergence

Inability to converge/ diverge in response to relevant target

Distinct convergence centre in midbrain/ divergence centre in pons

Nystagmus in Supranuclear Disorders

Types: Jerk, pendular, upbeat, downbeat.

Common Findings:

INO: Abducting nystagmus.

Parinaud’s: Convergence-retraction nystagmus.

Skew Deviation: Vestibular nystagmus.

Parkinson’s: Saccadic intrusions

2 sings of MS

INO
optic neuritis

whats the horizontal gaze centre?

PPRF
paramediun pontine reticular formation

what's the vertical gaze centre?

riMLF
rostral interstitial MLF

• Supranuclear: Refers to eye movement disorders where lesions occur above the cranial nerve nuclei.

• Internuclear: Between nuclei, typically involving the Medial Longitudinal Fasciculus (MLF), which coordinates eye movement between cranial nerve nuclei.

Anatomy and pathway

• Cranial Nerves:

  • III Nerve: Midbrain level (for medial rectus, superior rectus, inferior rectus, inferior oblique).

  • IV Nerve: Lower midbrain (superior oblique).

  • VI Nerve: Lower pons (lateral rectus).

  • The MLF connects III and VI for horizontal gaze coordination.

  • Vestibulo-Ocular Reflex (VOR): Initiated by head movement, detected by inner ear otoliths, signals eye movement opposite to head motion via VIII nerve to brainstem (no cortical involvement).

gaze centre

• Vertical Gaze (RiMLF)

  • Neural Integrators INC for vertical gaze,

• Horizontal Gaze (PPRF) centers, coordinating respective eye movements via cranial nerve nuclei.

  • NPH - nucleus prepositus hypoglossi for horizontal gaze hold gaze stable.

eye movement systems

• Saccades: Quick eye movements, processed in the cortical structures and coordinated through basal ganglia.

• Smooth Pursuit: Allows tracking of a moving target.

• Vestibulo-Ocular Reflex (VOR): Reflexive response to head movement, independent of cortical inpu

supranuclear lesions

Common Causes: Stroke, multiple sclerosis (MS), tumor, infection.

Supranuclear lesions affect gaze stability, leading to disruptions in smooth pursuit, saccades, or VOR, and can also affect pupils and eyelids.

internuclear lesions

• Multiple Sclerosis (MS) (most common in young adults).

• Brainstem Stroke (e.g., pontine infarcts).

• Trauma to the brainstem.

• Tumors in the brainstem.

• Infections (e.g., encephalitis).

Effects of Internuclear Lesions

• Disrupt communication between cranial nerve nuclei via the medial longitudinal fasciculus (MLF).

• Leads to Internuclear Ophthalmoplegia (INO):

  • Impaired adduction of the affected eye during contralateral gaze.

  • Abducting nystagmus in the contralateral eye.

• Vertical Gaze Palsy: If bilateral lesions affect the MLF.

• Can involve associated symptoms depending on the underlying cause (e.g., ataxia, weakness).

Distinctive Features

• Convergence typically spared in INO, distinguishing it from 3rd nerve palsy.

• Bilateral INO (common in MS) may present as "wall-eyed bilateral INO" (WEBINO).